immunology Flashcards

1
Q

list the PMNs (polymorphonuclear leukocytes)

A

neutrophils, basophils, and eosinophils

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2
Q

list the 3 key functional features of the immune system

A

discrimination: self vs nonself
memory
specificity: discern between different foreign antigens

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3
Q

innate vs adaptive cells and discrimination

result of ineffective discrimination?

A

innate system: discrimination is germline encoded, they are created already able to discriminate between self and nonself
adaptive: learn discrimination early in maturation
if body can no longer discriminate this is called autoimmunity

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4
Q

neutrophil mechanism of phagocytosis

A

PRR (pattern recognition receptor) identify PAMPs (pathogen associated molecular patterns), nutrophils express receptors for many bacterial and fungal constituents (LPS receptor, mannose receptor, N-formyl-Met receptor, CR3, scavenger receptor, glycan receptor, CR4 receptor). the neutrophils bind bacteria, engulf them and destroy them with the toxic contents of the neutrophil granules

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5
Q

TLR1 antigen

A

Lipopeptides

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6
Q

TLR2 antigen

A

gram positive (peptidoglycan), lipoteichoic acid, glycolipids, zymosan (fungi)

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7
Q

TLR3 antigen

A

double stranded viral RNA

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8
Q

TLR4 antigen

A

LPS, gram negative, heme

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9
Q

TLR5 antigen

A

flagellated bacteria (flagellin

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10
Q

TLR7 and TLR8 antigen

A

single stranded viral RNAs

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11
Q

TLR9 antigen

A

unmethylated CpG-rich DNA (bacteria, virus DNA)

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12
Q

mecahnism of TLR activation

A

TLR activation –> IFN-alpha and IFN-beta release–> induce resitance to viral replication in all cells, increased expression of ligands for receptors on NK cells, activate NK cells to kill virus-infected cells

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13
Q

TNF-alpha function

A

activates macrophages, increase vascular permeability

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14
Q

interferons function

A

block spread of viruses to uninfected cells, increase MHC class I, activates NK cells

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15
Q

endogenous pyrogens

A

increase the thermoregulatory set point in hypothalamus

IL-1, IL-6, TNF-alpha

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16
Q

PNM vs Mononuclear cells in inflammation

A

PMN: immediate responders, actively phagocytic, short lived (neutrophils, basophils, eosinophils)
mononuclear cells: include monocytes and macrophages, remove tissue debris including PMN after they die

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17
Q

lifespan of sickle cells

A

20 days or less

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18
Q

complement is part of which branch of the immune system? adaptive or innate?

A

innate

19
Q

define infection

A

inflammatory process caused by disease-producing organisms

20
Q

define pathogenic organism

A

capable of producing disease

21
Q

define virulence

A

measure of severity of disease

22
Q

how do antigens become concentrated in lymph nodes

A

migration of activated antigen presenting cells (APCs)

lymph drainage carries antigen to LN

23
Q

primary lymphoid organs

A

bone marrow and thymus

24
Q

secondary lymphoid organs

A

spleen, lymph nodes, tonsils, Peyer’s patches, appendix, GALT, MALT

25
Q

where does lymphatic system empty

A

superior vena cava

26
Q

immunoglobulins

A

(Ig’s)
expressed on B cells
Ig receptor is on the BCR which binds antigens
antibodies are immunoglobulins and are secreted by b cells

27
Q

structure of antibody (chains and regions)

A

heavy chain and light chain
each have a variable region: antigen binding domains “Fab” that are specific to the Ig
each also has a constant region: define the Ig isotype “Fc”

28
Q

when, where, and how do antigen-binding sites become so variable

A

when developing in the bone marrow, Bcell’s immunoglobulin genes are rearranged; this step is essential for Bcell development

29
Q

IgA function

A

mucosal immunity, neonatal passive

30
Q

IgD function

A

receptor- naive Bcells

31
Q

IgE function

A

immediate hypersensitivity

parasite immunity

32
Q

IgG function

A

opsonization, ADCC, neutralization, Complement activation,

33
Q

IgM function

A

receptor- naive B cells

complement activation

34
Q

list effector functions of antibodies

A

neutralization: blocks antigen ability of binding to cell surface receptors and being endocytoced
opsonization: coating antigen, increaseing efficiency of phagocytosis via Fc receptors on phagocytic cells

antibody dependent cell-mediated cytotoxicity: increaseefficiency of NK cell-mediated lysis of target cell and IgE mediated helmenth destruction by eosinophils

complement activation

35
Q

where does complement take place

A

ECF

36
Q

3 outcomes of complement

A

recruitment of inflammatory cells: C3a, C5a

opsonization of pathogens: C3b binds to complement receptors on phagocytes –> opsonization of pathogen, removes immune complexes

killing pathogens: terminal complement components (C5b, C6-9) created membrane attack complex which lyses the pathogens and cells

37
Q

describe immune complex clearance via C3b

A

C3b binds immune complexes in circulation, CR1 receptors on erythrocytes binds the immune complexes via the C3b, spleen and liver remove complexes from the erythrocyte surface

38
Q

how can immune complex clearance become abnormal

A

complexes can evade phagocytiv cells due to differences in size, shape, charge, hemodynamic factors

phagocytic cells are unable to clear bc of overwhelming numbers or dysfunctional mononuclear phagocytic system

39
Q

where do immune complexes most often get deposited

A

filtration sites

40
Q

steps in immune complex disease

A
  1. complex build up and deposition
  2. complement fixation
  3. recruit inflammatory cells
  4. vascular permeability
  5. tissue damage
  6. inflammation
41
Q

what deposits are found in acute glomerulonephritis

A

granular deposits of IgG and C3b on the GBM

42
Q

what is at abnormally low levels in acute glomerulonephritis

A

C3, C1

43
Q

what causes the decreased GFR in acute glomerulonephritis

A

proliferation of cells within the glomeruli, extracellular matrix and GBM are thickened